Previous work has established that the pathway by which cells are coupled to one another can be gated in much the same way that other smaller channels in biological membranes are regulated. Certain gap junctions possess voltage sensitivity of the same magnitude as in sodium channels of excitable cells although with much slower kinetics. Most, if not all gap junctions are gated by intracellular pH. The goal of the past year has been to determine the stoichiometry of the pH-conductance relation, to develop on-line methods for computation of steady state and kinetic properties of the voltage sensitivity as well as for fluctuation analysis of current noise under voltage clamp, and to obtain preliminary data concerning the temperature dependence of voltage sensitivity and the modifiability of conductance and gating mechanisms by application of various pharmacological agents. These studies are beginning to bridge the gap between molecular studies of gap junction polypeptides and the role of the gap junction in cell-cell communication and electrical coupling. The dramatic relation between junctional conductance and intracellular pH provides a plausible basis for reduced cardiac output during myocardial ischemia, the sensitivity of junctional conductance to transjunctional voltage may provide a novel operator in the control of differentiation and development. Further study of these and other controls on gap junction conductance should shed new light on this important communicant pathway and may even suggest novel therapeutic avenues in treatment of certain diseases.